Everett, Simon M.; Singh, Raj; Leuratti, Chiara; White, Kay L. M.; Neville, Peter; Greenwood, Darren; Marnett, Lawrence J.; Schorah, Christopher J.; Forman, David; Shuker, David and Axon, Anthony T. R.
Levels of Malondialdehyde-Deoxyguanosine in the gastric mucosa: Relationship with lipid peroxidation, ascorbic acid, and Helicobacter pylori.
Cancer Epidemiology Biomarkers & Prevention, 10(4) pp. 369–376.
Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M1-dG). We aimed to determine gastric mucosal levels of M1-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M1-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M1-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/108 bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 µmol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 µmol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M1-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M1-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/108 bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/108 bases; P = 0.8; n = 13) after successful eradication of H. pylori. M1-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.
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